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. 2023 Oct 19;14:1260839. doi: 10.3389/fimmu.2023.1260839

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Copyright © 2023 Zhao, Tang, Wang, Zhao and Zhu

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Ferroptosis mechanism: Ferroptosis is mainly caused by iron-dependent lipid peroxidation. It is mainly divided into ferroptosis promotion pathway (blue) and ferroptosis inhibition pathway (purple) (1). Iron metabolic pathway (2). Cystine/glutamate (also known as Xc-system)-GSH-GPX4 pathway: Cystine is imported into cells via the Xc-system, where it is oxidized to cysteine (Cys), followed by the synthesis of glutathione (GSH) in the presence of glutamate-cysteine ligase (GCL) and glutathione synthase (GSS). GSH is a potent reducing agent. GPX4 inhibits ferroptosis by using GSH as a reducing cofactor to reduce lipid hydroperoxides to lipid alcohols (3). Mevalonate pathway: Acetyl coenzyme A is first converted to HMG-CoA, which is then reduced to mevalonate by HMGCR, and mevalonate is converted to IPP. Finally, selenocysteine residues are added to the catalytic center of GPX4 to activate GPX4. At the same time, IPP can also produce coenzyme Q10 and then enter the FSP1 pathway (4). Lipid metabolic pathway: PUFAs are metabolized by ACSL4 and LPCAT3 and then oxidized by lipoxygenase HMGCR, 3-hydroxy-3-methylglutaryl coenzyme A reductase; IPP, isopentenyl pyrophosphate; GPX4, glutathione peroxidase 4; SLC1A5, solute carrier family 1 member 5; GLS, glutaminase; SLC3A2, solute carrier family 3 member 2. SLC7A11, solute carrier family 7 member 11; GSH, glutathione; Xc- system: glutamate reverse transporter protein, GPX4: glutathione peroxidase 4.